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Abstract Acute myeloid leulemia (AML) is a heterogenous disease clinically, morphologically and genetically, with accumulation of acquired genetic alterations in the hematopoietic progenitor cells resulting in clonal expansion of myeloid blasts in the bone marrow with a variable reduction in the production of normal of red blood cells platelets and mature granulocytes.In recent years, a number of molecular genetic alterations such as gene mutations and deregulated expression of genes have been identified, illustrating the enormous heterogeneity of acute myeloid leukemia , in particular in the large subset of AML exhibiting a normal karyotype .Nucleophosmin (NPM1), a protein that shuttles between the nucleus and cytoplasm, is most prominent in the nucleoli. NPM1 is responsible for prevention protein aggregation in the nucleolus and regulates the assembly and transport of preribosomal particles through the nuclear membrane.The NPM1 gene is a partner in the chromosomal translocation of leukemias and lymphomas that result in the formation of fusion protein.NPM1 appears to contribute to oncogenesis by activating the oncogenic potential of the fused protein partner. |